Evidence map›Paper›PMID 20071464›Full record

ArticleAmerican journal of physiology. Renal physiology2010

Dietary fructose causes tubulointerstitial injury in the normal rat kidney.

Takahiro Nakayama, Tomoki Kosugi, Michael Gersch, Thomas Connor, Laura Gabriela Sanchez-Lozada, Miguel A Lanaspa, Carlos Roncal, Santos E Perez-Pozo, Richard J Johnson, Takahiko Nakagawa

Abstract readComparative Study
In one paragraph

Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
5.9field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

85 citing papers in PubMed, 172 citations in OpenAlex.

  1. Trial
  2. Effects ofPharmaceuticals (Basel, Switzerland) · 2026
    Article
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  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
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  12. Fructokinase Inhibition to Prevent Kidney Disease.Clinical journal of the American Society of Nephrology : CJASN · 2024
    Article
  13. Review
  14. Article
  15. The fructose survival hypothesis for obesity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  16. Review
  17. Article
  18. Article
  19. Antihypertensive, antidyslipidemic, and renoprotective effects ofIranian journal of basic medical sciences · 2023
    Article
  20. Article

25 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 3 countries.

Takahiro NakayamaDivision of Nephrology, University of Florida, Gainesville, Florida, USA.
Tomoki Kosugi
Michael Gersch
Thomas Connor
Laura Gabriela Sanchez-Lozada
Miguel A Lanaspa
Carlos Roncal
Santos E Perez-Pozo
Richard J Johnson
Takahiko Nakagawa
University of Colorado Denver · USUniversity of Florida · USHospital General Mateu Orfila · ES

Funding

Role of Uric Acid in Hypertension and Renal DiseaseR01HL068607 · NHLBI · UNIVERSITY OF FLORIDA · PI JOHNSON, RICHARD JOSEPH · 2002 to 2011
$3.5M
NHLBI NIH HHS R01 HL-68607-01
6 · The paper itself

Abstract

Recent studies suggest that the metabolic syndrome is associated with renal disease. We previously reported that a high-fructose diet, but not a high-glucose diet, can induce metabolic syndrome and accelerate chronic renal disease in rats. We now examined the effects of a high-fructose diet on normal rat kidneys. Three groups of Sprague-Dawley rats were pair fed a special diet containing 60% fructose, 60% glucose, or control standard rat chow for 6 wk, and then histological studies were performed. The effect of fructose to induce cell proliferation in cultured proximal tubular cells was also performed. Fructose diet, but not glucose diet, significantly increased kidney weight by 6 wk. The primary finding was tubular hyperplasia and proliferation involving all segments of the proximal tubules while glomerular changes were not observed. This is the same site where the fructose transporters (GLUT2 and -5) as well as the key enzyme in fructose metabolism (ketohexokinase) were expressed. Consistently, fructose also induced proliferation of rat proximal tubular cells in culture. In vivo, tubular proliferation was also associated with focal tubular injury, with type III collagen deposition in the interstitium, an increase in alpha-smooth muscle actin positive myofibroblasts, and an increase in macrophage infiltration. In conclusion, a high-fructose diet induces cell proliferation and hyperplasia in proximal tubules, perhaps via a direct metabolic effect. The effect is independent of total energy intake and is associated with focal tubulointerstitial injury. These studies may provide a mechanism by which metabolic syndrome causes renal disease.

Indexed as

ActinsAnimalsCell ProliferationCells, CulturedCollagenDietary SucroseFibroblastsFructokinasesFructoseGlucoseGlucose Transporter Type 2Glucose Transporter Type 5HyperplasiaKidney DiseasesKidney Tubules, ProximalMacrophagesActa2 protein, ratActinsCollagenDietary SucroseFructokinasesFructoseGlucoseGlucose Transporter Type 2Glucose Transporter Type 5ketohexokinaseSlc2a2 protein, ratSlc2a5 protein, rat

Identifiers

PMID20071464
PMCPMC2838595
OpenAlexW2120390687

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.